Parameters of nitrogen metabolism during insulin hypoglycemia in rats with alloxan-induced diabetes.

Hypoglycemic coma caused by insulin injection to rats with alloxan-induced diabetes was accompanied by an increase in the concentrations of urea and uric acid and decrease in the content of free amino acids in blood plasma. Activities of glutamate dehydrogenase, AMP deaminase, glutaminase, ALT, and AST in the liver of experimental animals increased.

[Changes of some energy exchange parameters in the rat heart under insulin hypoglycemia].

Hypoglycemic coma induced by administration of a large dose of insulin, was accompanied by the increased rates of glycolysis, glycogenolysis, activity of lactate dehydrogenase, succinate dehydrogenase, isocitrate dehydrogenase, and increased concentration of glycogen. Under these conditions triacylglycerol content decreased administration of the large dose of insulin to rats with alloxan diabetes increased not only rates of glycolysis, glycogenolysis and lactate dehydrogenase activity and also activities of aspartate transaminase and glutamate dehydrogenase. Data obtained suggest the increased utilization of amino acids for energy supply of myocardium under conditions of hypoglycemia induced by insulin adminisration to diabetic animals.

[Rat metabolic parameters in multiple insulin hy- 44poglycemia].

Hypoglycemic coma was induced with 40 U of insulin per kg body weight. The animals experiencing 7 hypoglycemic comas at 2-day intervals and killed during the last coma were found to have elevated serum levels of free fatty acids, urea, and uric acid; hepatic glycogen levels remained normal. In the liver, the activities of aspartate aminotransferase (EC 2.6.1.1), alanine aminotransferase (EC 2.6.1.2), glutaminase (EC 3.5.1.2), glutamate dehydrogenase (EC 1.4.1.3), succinate dehydrogenase (EC 1.3.99.1), and lactate dehydrogenase (EC 1.1.1.27) were enhanced and the rate of lactate generation increased when glucose and glycogen were used as substrates. Such changes were absent in initially healthy animals during the first hypoglycemic coma. They are indicative of increases in the catabolism of amino acids and in the activation of gluconeogenesls in the rats experiencing insulin hypoglycemia many times and they are associated with the stimulation of the contramsular apparatus in hypoglycemia.

Glycolysis and oxidtion enzyme activity in rat brain during insulin-induced hypoglycemia against the background of alloxan-induced diabetes mellitus.

Insulin-induced hypoglycemic coma in animals with alloxan diabetes was observed at a higher basal glucose level in the blood compared to healthy animals. It was associated with inhibition of glycolysis and glycogenolysis and decreased activities of succinate dehydrogenase and glutamate dehydrogenase in the cerebral hemispheres and brainstem.